Many tumours express antigens which may serve as a target or therapy. Such antigens can be broadly divided into:                oncogenes, such as the MAGE identified in some melanomas;        proto-oncogenes, such as cyclin D1 expressed on soft tissues carcinomas such as those of the kidney or parathyroid, as well as in multiple myeloma;        virus-derived proteins, such as those from the Epstein-Barr virus in some carcinomas and in some Hodgkin-type lymphomas;        surviving factors, which are anti-apoptotic factors such as survivin or bcl2; and        clonotypic determinants, such as idiotypic determinants derived from B cell receptor in follicular lymphomas or multiple myelomas or T cell receptor determinants in T cell malignancies.        
Specific recognition of such antigens, expressed exclusively or predominantly in tumour cells, offers the potential of a selective elimination of such cells. Active immunisation with tumour-associated antigens or derivatives, or adoptive transfer of cells expanded in vitro with such tumour-associated antigens could in theory be of interest for the therapy of tumours. Over recent years, many attempts to elicit tumour-specific elimination by specific immunotherapy have been published. These included active immunisation with, for example, idiotype-derived peptides, as well as adoptive transfer of T cells expanded in vitro by exposure to tumour cells. Although very promising, these therapeutic approaches had limited success and/or were associated with a high rate of relapse. Besides, the capacity of T cells to undergo expansion in vitro remains limited, with much loss of effector cells by apoptosis induced by overstimulation. Essentially all the work carried out in the field of immunotherapy of tumours during the last 15 years has been devoted to methods to elicit cytolytic CD8+ T cells able to recognise and lyse tumour cells in a MHC class I dependent presentation of a tumour-derived antigen. The possibility of designing efficient immunotherapy through MHC class II presentation of tumour-derived peptides and CD4+ T cells has not been explored until very recently (Perez-Diez et al. (2007), Blood 109, 5346-5354). This is imputable to several factors, including the widespread belief that most tumours do not express MHC class II determinants and that the function of CD4+ T cells does not predispose them to be potent anti-tumour cells. The classical view is that CD4+ T cells can help in providing help to B cells to produce specific antibodies and that the production of IFN-gamma by Th1 CD4+ T cells could reduce angiogenesis. More recently, the requirement of CD4+ T cells as a source of IL-2 to help CD8+ T cells to acquire full maturation has been described.
Despite major advances in the field of cancer treatment, immunotherapy of tumours is still in its infancy. The potential selectivity of such immunotherapy, certainly when targeting tumour-specific antigens, is an important advantage and may eliminate the sometimes severe side effects observed with e.g. chemotherapy. Therefore, any new strategy for immunotherapeutic treatment of cancer would be welcomed.